Mechanisms of aging in senescence-accelerated mice
Open accessAbstract
Background: Progressive neurological dysfunction is a key aspect of human aging. Because of underlying differences in the aging of mice and humans, useful mouse models have been difficult to obtain and study. We have used gene-expression analysis and polymorphism screening to study molecular senescence of the retina and hippocampus in two rare inbred mouse models of accelerated neurological senescence (SAMP8 and SAMP10) that closely mimic human neurological aging, and in a related normal strain (SAMR1) and an unrelated normal strain (C57BL/6J). Results: The majority of age-related gene expression changes were strain-specific, with only a few common pathways found for normal and accelerated neurological aging. Polymorphism screening led to the identification of mutations that could have a direct impact on important disease processes, including a mutation in a fibroblast growth factor gene, Fgf1, and a mutation in and ectopic expression of the gene for the chemokine CCL19, which is involved in the inflammatory response. Conclusion: We show that combining the study of inbred mouse strains with interesting traits and gene-expression profiling can lead to the discovery of genes important for complex phenotypes. Furthermore, full-genome polymorphism detection, sequencing and gene-expression profiling of inbred mouse strains with interesting phenotypic differences may provide unique insights into the molecular genetics of late-manifesting complex diseases.
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Retinal expression profiles of senescence-accelerated mice highlighted expression changes for a different set of genes.
“Retinal expression profiles of senescence-accelerated mice highlighted expression changes for a different set of genes (21).”
From Unraveling a Multifactorial Late-Onset Disease: From Genetic Susceptibility to Disease Mechanisms for Age-Related Macular Degeneration (2009) · cites this paper as [21]
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- Authors
- Carter, T. A., Greenhall, J. A., Yoshida, S., Fuchs, S., Helton, R., Swaroop, A., Lockhart, D. J., & Barlow, C.
- Affiliations
- Salk Institute for Biological Studies (US)
- University of Michigan (US)
- Corresponding author
- Barlow, Carrolee
- Venue
- Genome Biology
- Published
- 2005-06-01
- Volume
- 6
- Issue
- 6
- Pages
- R48-R48
- ISSN
- 1465-6906 (ISSN-L)
- 1474-760X
- PMC
- PMC1175968
- OpenAlex
- W2161839034
- Cited by
- 64
- References
- 60
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 2 · 2023: 3 · 2022: 4 · 2021: 3 · 2020: 6 · 2018: 3 · 2017: 6 · 2016: 1 · 2015: 1 · 2014: 3 · 2013: 4 · 2012: 1
- FWCI
- 1.31
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Genome biology (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Defense
- Foundation for the National Institutes of Health
- Macula Vision Research Foundation
- National Institutes of Health
- National Defense Science and Engineering Graduate
- National Eye Institute (EY11115, R01EY011115)
- National Cancer Institute (CA-09370, T32CA009370)
- National Institute of Neurological Disorders and Stroke (R01NS039601, 5-R01 NS039601-04)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Antioxidants, Aging, Portulaca oleracea
- Keywords
- senescence-accelerated mice, SAMP8 mice, SAMR1, C57BL/6J mice, accelerated aging, retina, hippocampus, gene expression profiling, genetic polymorphism, FGF1, CCL19, chemokines, fibroblast growth factor
- MeSH terms
- Aging, Amino Acid Sequence, Animals, Brain, Mice, Inbred AKR, Mice, Inbred C57BL, Mice, Mutant Strains, Molecular Sequence Data, Mutation, Nervous System, Phenotype, Retina, RNA, Messenger, Species Specificity, Fibroblast Growth Factor 1, Chemokines, CC, Gene Expression Profiling, Chromosomes, Mammalian, Mice, Chemokine CCL19
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